No treatments exist which have been proven to modify the course of scleroderma, a disease with median life expectancy of less than 10 years. Experimental evidence has implicated ischemia-reperfusion-induced injury, metal-catalyzed modifications of autoantigen structure, and excess fibroblast collagen production in the pathogenesis of this disease. Zinc has been shown in vitro to inhibit each of these processes. Zinc has been used safely for the treatment of other conditions, notably Wilson's Disease, but the safety of zinc therapy in scleroderma patients remains to be established. The aim of this study is to assess the safety and bioavailability of oral zinc sulfate in scleroderma patients. Using a dosing regimen common to Wilson's Disease therapy, patients with diffuse scleroderma will be monitored clinically for adverse events as the primary study outcome over a 6-week trial. To date, there have been no significant adverse events, and no prptocol dropouts. Mean increases in serum zinc levels in scleroderma patients have been observed, consistent with those seen in other populations. Two of four patients to complete the study protocol have elected to continue taking zinc at the conclusion of the study protocol due to a subjective sense of benefit. Mean improvements in patient and physician global visual analogue scale scores, health assessment questionnaire scores, and modified Rodnan skin scores have been observed. Measures of cutaneous fibroblast zinc levels before and after zinc therapy are pending. If zinc is safe and bioavailable when administered to scleroderma pateints, it holds promise as an agent which may favorably alter the clinical course of scleroderma.